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Effects of Metabolic Inhibition and Acidosis on the Contractility of the Pulmonay and Ear Artery

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dc.contributor.authorPark, Myoung Kyu-
dc.contributor.authorEarm, Yung E-
dc.date.accessioned2009-08-20T05:37:20Z-
dc.date.available2009-08-20T05:37:20Z-
dc.date.issued1994-12-
dc.identifier.citationSeoul J Med, Vol.35 No.4, pp. 231-237-
dc.identifier.issn0582-6802-
dc.identifier.urihttps://hdl.handle.net/10371/7353-
dc.description.abstractHypoxia causes contraction in pulmonary artery, whereas it causes
relaxation in systemic artery. The purpose of this study is to test whether pulmonary
artery would respond to metabolic inhibition and acidosis differently from ear artery.
Rabbit pulmonary artery and ear artery were precontracted with phenylephrine or
KCI, and then exposed to metabolic blockers (dlnttrophenof Hrlvl'), Na-cyanide
(NaCN)) and acidosis. Contractile forces of ear artery induced by 30mM KCI and
1O-6M phenylephrine were 2-3times(n =7) and 5-9 times (n = 7) larger than that of
the pulmonary artery, respectively, DNP and NaCN produced a dose-dependent
relaxation in the pulmonary and ear artery, and the relaxation was more profound in
the ear artery than in pulmonary artery. This effect was independent of the presence
of the endothelium. Extracellular acidosis reduced the tone of the KCI-induced
contraction, more in the ear artery than in pulmonary artery. These results indicate
that pulmonary artery is more resistant to both of the inhibition of metabolism and
acidosis than ear artery.
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dc.language.isoen-
dc.publisherSeoul National University College of Medicine-
dc.subjectPulmonary artery-
dc.subjectEar artery-
dc.subjectHypoxic pulmonary vasoconstriction-
dc.subjectDNP-
dc.subjectCyanide-
dc.subjectacidosis-
dc.titleEffects of Metabolic Inhibition and Acidosis on the Contractility of the Pulmonay and Ear Artery-
dc.typeSNU Journal-
dc.contributor.AlternativeAuthor박명규-
dc.contributor.AlternativeAuthor엄융의-
dc.citation.journaltitle서울 의대 잡지-
dc.citation.journaltitle서울 의대 학술지-
dc.citation.journaltitleSeoul Journal of Medicine-
dc.citation.endpage237-
dc.citation.number4-
dc.citation.pages231-237-
dc.citation.startpage231-
dc.citation.volume35-
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